256
ryanodine receptor also occurs. BPA also causes an increase in phospholipase C
activation, triphosphoinositol (IP 3 ) production, and release of calcium-mediated by
IP 3 receptor. Phosphorylation of the ryanodine receptor increases the leakage of
calcium from sarcoplasmic reticulum due to the opening of calcium channels.
Activation of calcium-dependent protein kinase II causes the phosphorylation of
phospholamban which inhibits the calcium release from endoplasmic reticulum
Ca
2+
-ATPase and increases the uptake. These pathways cause arrhythmogenesis in
myocytes [28].
BPA Effect on the Liver
The liver plays a key role in the regulation of glucose metabolism via hepatic glucose production. In addition, the liver is the main organ responsible for the detoxification of chemicals that are present in the whole body as the center of the
metabolism of toxic substances, drugs, xenobiotics, and environmental hormones.
BPA, belonging to environmental xenobiotic contaminants, reaches the liver where
it gets metabolized [34]. BPA has the ability to damage the cells in the liver due to
oxidative stress. BPA has significantly reduced the level of antioxidant enzymes and
glutathione levels due to a reduction in the activities of glutathione-S-transferase.
Due to high exposure of BPA, increased sufficiently the concentration of the
enzymes in the liver and also increased the activity of the antioxidant genes in the
tissues of the liver. The research has proved that reactive oxygen species increased
due to BPA exposure and also causes a reduction in the expression of genes, ultimately responsible for hepatotoxicity [6]. The low concentration of BPA can also
cause hepatotoxicity which may be due to disturbance in the function of the mitochondria, abnormality in the production of reactive oxygen species, hyperpolarization of the mitochondrial membrane, oxidation of lipids, and release of the cytokines
[35]. Another study also shows that oxidation of the lipids decreases the level of
glutathione peroxidase, pro-inflammatory cytokines including the tumor necrosis
factor and interleukin 6. Exposure of BPA in very low concentration has also an
effect on decreasing the oxygen level, production of ATP, and disturbs the function
of the mitochondria that is present in the liver cells [36].
BPA Effect on the Immune System
BPA has an effect on the estrogenic receptors due to which it has the ability to
induce modulation in the immune system functions. BPA has also the ability to bind
with aryl hydrocarbon receptor and peroxisome proliferator-activated receptor. BPA
has the capability to stimulate and inhibit the activity of the cells in the immune
system [37]. Due to exposure of BPA, the amount of T lymphocytes is increased and
as a result, the level of interferon increases while interleukin level is decreased [38].
K. Irshad et al.
ryanodine receptor also occurs. BPA also causes an increase in phospholipase C
activation, triphosphoinositol (IP 3 ) production, and release of calcium-mediated by
IP 3 receptor. Phosphorylation of the ryanodine receptor increases the leakage of
calcium from sarcoplasmic reticulum due to the opening of calcium channels.
Activation of calcium-dependent protein kinase II causes the phosphorylation of
phospholamban which inhibits the calcium release from endoplasmic reticulum
Ca
2+
-ATPase and increases the uptake. These pathways cause arrhythmogenesis in
myocytes [28].
BPA Effect on the Liver
The liver plays a key role in the regulation of glucose metabolism via hepatic glucose production. In addition, the liver is the main organ responsible for the detoxification of chemicals that are present in the whole body as the center of the
metabolism of toxic substances, drugs, xenobiotics, and environmental hormones.
BPA, belonging to environmental xenobiotic contaminants, reaches the liver where
it gets metabolized [34]. BPA has the ability to damage the cells in the liver due to
oxidative stress. BPA has significantly reduced the level of antioxidant enzymes and
glutathione levels due to a reduction in the activities of glutathione-S-transferase.
Due to high exposure of BPA, increased sufficiently the concentration of the
enzymes in the liver and also increased the activity of the antioxidant genes in the
tissues of the liver. The research has proved that reactive oxygen species increased
due to BPA exposure and also causes a reduction in the expression of genes, ultimately responsible for hepatotoxicity [6]. The low concentration of BPA can also
cause hepatotoxicity which may be due to disturbance in the function of the mitochondria, abnormality in the production of reactive oxygen species, hyperpolarization of the mitochondrial membrane, oxidation of lipids, and release of the cytokines
[35]. Another study also shows that oxidation of the lipids decreases the level of
glutathione peroxidase, pro-inflammatory cytokines including the tumor necrosis
factor and interleukin 6. Exposure of BPA in very low concentration has also an
effect on decreasing the oxygen level, production of ATP, and disturbs the function
of the mitochondria that is present in the liver cells [36].
BPA Effect on the Immune System
BPA has an effect on the estrogenic receptors due to which it has the ability to
induce modulation in the immune system functions. BPA has also the ability to bind
with aryl hydrocarbon receptor and peroxisome proliferator-activated receptor. BPA
has the capability to stimulate and inhibit the activity of the cells in the immune
system [37]. Due to exposure of BPA, the amount of T lymphocytes is increased and
as a result, the level of interferon increases while interleukin level is decreased [38].
K. Irshad et al.